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Published in: Translational Stroke Research 6/2018

01-12-2018 | Original Article

ICAM-1null C57BL/6 Mice Are Not Protected from Experimental Ischemic Stroke

Authors: Gaby U. Enzmann, Sofia Pavlidou, Markus Vaas, Jan Klohs, Britta Engelhardt

Published in: Translational Stroke Research | Issue 6/2018

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Abstract

Accumulation of neutrophils in the brain is a hallmark of cerebral ischemia and considered central in exacerbating tissue injury. Intercellular adhesion molecule (ICAM)-1 is upregulated on brain endothelial cells after ischemic stroke and considered pivotal in neutrophil recruitment as ICAM-1-deficient mouse lines were found protected from experimental stroke. Translation of therapeutic inhibition of ICAM-1 into the clinic however failed. This prompted us to investigate stroke pathogenesis in Icam1tm1Alb C57BL/6 mutants, a true ICAM-1null mouse line. Performing transient middle cerebral artery occlusion, we found that absence of ICAM-1 did not ameliorate stroke pathology at acute time points after reperfusion. Near-infrared imaging showed comparable accumulation of neutrophils in the ischemic hemispheres of ICAM-1null and wild type C57BL/6 mice. We also isolated equal numbers of neutrophils from the ischemic brains of ICAM-1null and wild type C57BL/6 mice. Immunostaining of the brains showed neutrophils to equally accumulate in the leptomeninges and brain parenchymal vessels of ICAM-1null and wild type C57BL/6 mice. In addition, the lesion size was comparable in ICAM-1null and wild type mice. Our study demonstrates that absence of ICAM-1 neither inhibits cerebral ischemia-induced accumulation of neutrophils in the brain nor provides protection from ischemic stroke.
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Metadata
Title
ICAM-1null C57BL/6 Mice Are Not Protected from Experimental Ischemic Stroke
Authors
Gaby U. Enzmann
Sofia Pavlidou
Markus Vaas
Jan Klohs
Britta Engelhardt
Publication date
01-12-2018
Publisher
Springer US
Published in
Translational Stroke Research / Issue 6/2018
Print ISSN: 1868-4483
Electronic ISSN: 1868-601X
DOI
https://doi.org/10.1007/s12975-018-0612-4

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